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Epithelial barrier dysfunction and apoptosis resistance of immune cells have been proposed to contribute to the chronic inflammation seen in patients with inflammatory bowel disease. The soluble decoy receptor 3 (DcR3) inhibits death ligand-induced apoptosis. In the study by Funke and co-writers in this issue of Gut, the authors demonstrate that DcR3 is over-expressed in patients with Crohn’s disease (CD), both in the epithelial layer of ileum (see fig) and in serum. Moreover, this was seen both at active and non-active sites within the gut and present in patients with active and non-active disease. Furthermore, they could also demonstrate that DcR3 over-expression was associated with activation of nuclear factor kappa B (NF-
B), which is of interest because a deregulated activation of NF-B-dependent pro-survival signalling pathways may be involved in malignant transformation of enterocytes. The increased DcR3 expression was also found to protect against death ligand-induced apoptosis of
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